Dissimilar effects of LY 294002 and PD 098059 in IGF-I-mediated inhibition of TGF-beta1 expression and apoptosis in bovine mammary epithelial cells.

摘要: In mammary epithelial cells (MEC) TGF-beta(1) is the auto-/paracrine growth inhibitor and inducer of apoptosis therefore considered as an important local regulator tissue involution. However, mechanisms controlled expression in course bovine gland remodelling are still unclear. Recent study performed this laboratory support evidence that MEC regulated by hormones somatotropic axis (GH, IGF-I somatostatin). Present was focused on contribution IGF-I-induced signaling pathways anti-TGF-beta(1) anti-apoptotic effects IGF-I. Laser scanning cytometry applied for measurement content apoptotic cell number BME-UV1 MEC. Involution vitro modeled decreasing availability FBS Reducing medium from 10% to 0.5% evoked highly significant increase number. (50 ng/ml) completely abrogated deficiency-induced order establish which contributed effects, inhibitors PI3-kinase - (LY 294002) MEK- (MAPKK ERK) (PD 098059) mediated were our model. The results clearly showed inhibition PI3-K reverses ability suppress apoptosis. An ERK1/2 pathway even potentiated inhibitory effect expression, but partially conclusion, indicate PI3-K/Akt significantly IGF-I, whereas both involved